OBJECTIVE: To characterize the effect of focal compression by threshold tracking and other excitability measures of human median motor axons. METHODS: We conducted a sequence of excitability studies using a software written in BASIC (QTRAC version 4.0, (c)Institute of Neurology, London, UK, with multiple excitability protocol TRONDXM 2) in 24 healthy subjects, stimulating the median nerve at the wrist and recording compound muscle action potentials from the abductor pollicis brevis. Constant, localized compression was applied at the wrist by mechanically lowering a probe attached to a disk electrode, which also served as the stimulating cathode. RESULTS: Compared with the pre-compression values, measurements during compression showed a shift of threshold electrotonus waveforms toward the baseline (fanning-in), steeper current-threshold relationships, increased strength-duration time constants, prolonged relative refractory periods and reduced levels of superexcitability, but no alteration in late subexcitability. These excitability changes indicating depolarization reversed to hyperpolarization immediately after release of compression. The nerve compression altered none of the excitability measures when recorded 2 cm distally from the pressure probe. CONCLUSIONS: Mild nerve compression produces a very localized axonal depolarization at the compression site followed by hyperpolarization upon release of compression, as expected from focal ischemia. SIGNIFICANCE: The current results imply that the sharply-localized conduction abnormalities demonstrated electrophysiologically in peripheral nerve entrapment syndromes and compression myelopathies may, in part, result from compression-induced focal nerve ischemia.
OBJECTIVE: To characterize the effect of focal compression by threshold tracking and other excitability measures of human median motor axons. METHODS: We conducted a sequence of excitability studies using a software written in BASIC (QTRAC version 4.0, (c)Institute of Neurology, London, UK, with multiple excitability protocol TRONDXM 2) in 24 healthy subjects, stimulating the median nerve at the wrist and recording compound muscle action potentials from the abductor pollicis brevis. Constant, localized compression was applied at the wrist by mechanically lowering a probe attached to a disk electrode, which also served as the stimulating cathode. RESULTS: Compared with the pre-compression values, measurements during compression showed a shift of threshold electrotonus waveforms toward the baseline (fanning-in), steeper current-threshold relationships, increased strength-duration time constants, prolonged relative refractory periods and reduced levels of superexcitability, but no alteration in late subexcitability. These excitability changes indicating depolarization reversed to hyperpolarization immediately after release of compression. The nerve compression altered none of the excitability measures when recorded 2 cm distally from the pressure probe. CONCLUSIONS: Mild nerve compression produces a very localized axonal depolarization at the compression site followed by hyperpolarization upon release of compression, as expected from focal ischemia. SIGNIFICANCE: The current results imply that the sharply-localized conduction abnormalities demonstrated electrophysiologically in peripheral nerve entrapment syndromes and compression myelopathies may, in part, result from compression-induced focal nerve ischemia.